Skip to content

Repeated visual hallucinations in Parkinson's disease as disturbed external/internal perceptions: focused review and a new integrative model.

Nico J Diederich, Christopher G Goetz, Glenn T Stebbins

Movement Disorders February 2005 DOI: 10.1002/mds.20308 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Theoretical or philosophical paper Peer reviewed
Key points Proposes that visual hallucinations in Parkinson's disease reflect a dysregulation of gating and filtering between external perception and internally generated imagery, integrating factors such as poor primary vision, aberrant cortical activation, intrusion of REM dreaming imagery, fluctuating vigilance, and medication-related mesolimbic overactivation. Argues that different etiologies may produce different phenomenologies and prognoses, and that the model yields testable hypotheses.

Abstract

Visual hallucinations (VH) in Parkinson's disease (PD) are a chronic complication in 30 to 60% of treated patients and have a multifaceted phenomenology. Flickering, faultive impressions, and illusionary misperceptions precede the core syndrome of stereotyped, colorful images. The patient variably recognizes these images as hallucinations, being rarely irritated or frightened and more often amused as a bystander. Although studies on VH in PD focus on several research domains, no comprehensive, unified theory has been developed to study their pathophysiology. We have adapted Hobson's work on the states of consciousness and propose a model integrating seemingly disparate data on VH. We suggest that VH should be considered as a dysregulation of the gating and filtering of external perception and internal image production. Contributive elements and anatomical links for the model include poor primary vision, reduced activation of primary visual cortex, aberrant activation of associative visual and frontal cortex, lack of suppression or spontaneous emergence of internally generated imagery through the ponto-geniculo-occipital system, intrusion of rapid eye movement dreaming imagery into wakefulness, errative changes of the brainstem filtering capacities through fluctuating vigilance, and medication-related overactivation of mesolimbic systems. Different etiologies likely produce different phenomenologies and the prognosis may not be uniform. This new conceptual framework permits an anatomical view of VH and suggests new, testable hypotheses regarding their pathophysiology and therapy.

Citations in the library

Explore topics